Atopic diseases such as allergic asthma and atopic dermatitis are thought to involve a pathogenic shift to predominant Th2 immunity (Umetsu et al., 2002, Nat. Immunol. 3:715-20.
In the asthma setting Th2 cytokine production drives eosinophil influx into the lung, eosinophil activation, IgE production and IgE mediated mast cell activation and degranulation, and mononuclear cell accumulation in lung interstitial space, where T cells and activated granulocytes continue to secrete Th2 cytokines, chemokines, and effector molecules, thereby fostering continued lung inflammation. The TAPR locus containing the KIM gene family has been implicated in the development of atopic inflammation in mouse, and KIM-1 allelic variation has been associated with the incidence of atopy in patient population analyses (McIntire et al., 2001, Nat Immunol 2:1109-16; McIntire et al., 2003, Nature 425:576).